scholarly journals Long non-coding RNA cancer susceptibility candidate 2 (CASC2) alleviates the high glucose-induced injury of CIHP-1 cells via regulating miR-9-5p/PPARγ axis in diabetes nephropathy

2020 ◽  
Vol 12 (1) ◽  
Author(s):  
Feng Li ◽  
Bo Dai ◽  
Xiquan Ni
Keyword(s):  
High Glucose ◽  
Cancer Susceptibility ◽  
Non Coding Rna ◽  
Diabetes Nephropathy ◽  
Long Non Coding Rna

scholarly journals Retraction: Long non-coding RNA TUG1 alleviates high glucose induced podocyte inflammation, fibrosis and apoptosis in diabetic nephropathy via targeting the miR-27a-3p/E2F3 axis

RSC Advances ◽  
2021 ◽  
Vol 11 (9) ◽  
pp. 5244-5244
Author(s):  
Laura Fisher
Keyword(s):  
Diabetic Nephropathy ◽  
High Glucose ◽  
Non Coding Rna ◽  
Long Non Coding Rna

Retraction of ‘Long non-coding RNA TUG1 alleviates high glucose induced podocyte inflammation, fibrosis and apoptosis in diabetic nephropathy via targeting the miR-27a-3p/E2F3 axis’ by Yang Li et al., RSC Adv., 2019, 9, 37620–37629, DOI: 10.1039/C9RA06136C.

scholarly journals Association Between Long Non-Coding RNA POLR2E rs3787016 Polymorphism and Cancer Susceptibility: A Meta-analysis of 8725 Cancer Cases and 10710 Controls

2020 ◽  
Vol In Press (In Press) ◽  
Author(s):  
Saeid Ghavami ◽  
Mohsen Taheri ◽  
Mohammad Hashemi
Keyword(s):  
Breast Cancer ◽  
Web Of Science ◽  
Cancer Susceptibility ◽  
Meta Analysis ◽  
Positive Association ◽  
Cancer Development ◽  
Non Coding Rna ◽  
Stratified Analysis ◽  
The Relationship ◽  
Long Non Coding Rna

Objectives: Several studies have reported a correlation between the POLR2E rs3787016 polymorphism and cancer development, but findings are inconsistent. Therefore, we designed the current study to understand how rs3787016 polymorphism impacts cancer susceptibility. Methods: We searched the Scopus, Web of Science, and PubMed databases for studies related to the topic of interest published up to March 2019. A total of 11 relevant studies, encompassing 8,761 cancer cases and 10,534 controls, were retrieved and subject to quantitative analysis. The strength of the relationship was evaluated using the pooled odds ratios (ORs) with 95% confidence intervals (CIs). Results: Overall, the findings proposed a positive association between rs189037 polymorphism and susceptibility to cancer in homozygous (OR = 1.32, 95% CI = 1.11 - 1.57, P = 0.002, TT vs. CC), recessive (OR = 1.21, 95% CI = 1.06-1.39, P = 0.005, TT vs. CT + CC), and allele (OR = 1.12, 95% CI = 1.02-1.22, P = 0.021, T vs. C) genetic models. Stratified analysis showed that rs3787016 increased the risk of prostate and breast cancer. In addition, we found a significant association between the variant and increased cancer risk in Asian and Caucasian populations. Conclusions: In summary, the findings of the current meta-analysis suggest that the POLR2E rs3787016 polymorphism is an indicator of cancer susceptibility.

scholarly journals Significant association between long non-coding RNA H19 polymorphisms and cancer susceptibility

Medicine ◽  
2020 ◽  
Vol 99 (15) ◽  
pp. e19322 ◽  
Author(s):  
Wei Li ◽  
Xia Jiang ◽  
Xiaojing Jin ◽  
Weitao Yan ◽  
Ying Liu ◽  
...  
Keyword(s):  
Cancer Susceptibility ◽  
Non Coding Rna ◽  
Long Non Coding Rna

scholarly journals Long non-coding RNA MEG3 serves as a ceRNA for microRNA-145 to induce apoptosis of AC16 cardiomyocytes under high glucose condition

2019 ◽  
Vol 39 (6) ◽  
Author(s):  
Yiwei Chen ◽  
Zhifang Zhang ◽  
Diqi Zhu ◽  
Wenchuo Zhao ◽  
Fen Li
Keyword(s):  
High Glucose ◽  
Human Cardiomyocytes ◽  
Non Coding Rna ◽  
High Glucose Condition ◽  
Promising Therapeutic Target ◽  
Underlying Mechanisms ◽  
Induced Apoptosis ◽  
Long Non Coding Rna ◽  
Glucose Condition

AbstractDiabetic cardiomyopathy (DCM) is one of the most serious complications of diabetes, but its pathogenesis remains largely unclear. In the present study, we aimed to explore the potential role of long non-coding RNA (lncRNA) maternally expressed gene 3 (MEG3) and to investigate the underlying mechanisms in human AC16 cardiomyocytes under high glucose (HG) condition. The results demonstrated that MEG3 was overexpressed in HG-treated AC16 cells, and MEG3 knockdown suppressed the HG-induced apoptosis in AC16 cells. Mechanistically, MEG3 directly binds to miR-145 in AC16 cells, thereby up-regulating the expression of PDCD4. Rescue experiments showed that the role of MEG3 in HG-treated AC16 cells was partly dependent on its suppression on miR-145. In summary, our findings suggested that the role of MEG3 in HG-treated human cardiomyocytes is to serve as a competing endogenous RNA (ceRNA), which negatively regulates miR-145. These findings may provide a valuable and promising therapeutic target for the treatment of DCM in the future.

scholarly journals Long non-coding RNA CDKN2B-AS1 regulates high glucose-induced human mesangial cell injury via regulating the miR-15b-5p/WNT2B axis

2020 ◽  
Vol 12 (1) ◽  
Author(s):  
Jing Chang ◽  
Yanming Yu ◽  
Zhan Fang ◽  
Haiyan He ◽  
Dan Wang ◽  
...  
Keyword(s):  
Cell Cycle ◽  
High Glucose ◽  
Cell Cycle Progression ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Enzyme Linked Immunosorbent Assay ◽  
Cycle Progression ◽  
Inflammation Response ◽  
Non Coding Rna ◽  
Long Non Coding Rna

Abstract Background Long non-coding RNA cyclin-dependent kinase inhibitor 2B antisense RNA 1 (CDKN2B-AS1) has been reported to be related to diabetic nephropathy (DN) progression. However, the regulatory mechanisms of CDKN2B-AS1 in DN are unclear. Methods High glucose (HG) was used to induce human mesangial cells (HMCs) for establishing the DN model. Expression levels of CDKN2B-AS1, microRNA (miR)-15b-5p, wingless-Type family member 2B (WNT2B) mRNA in serum and HMCs were detected through quantitative real-time polymerase chain reaction (qRT-PCR). The viability and cell cycle progression of HMCs were determined with Cell Counting Kit-8 (CCK-8) or flow cytometry assays. The levels of several proteins and inflammatory factors in HMCs were analyzed by western blotting or enzyme-linked immunosorbent assay (ELISA). The relationship between CDKN2B-AS1 or WNT2B and miR-15b-5p was verified with dual-luciferase reporter assay. Results CDKN2B-AS1 and WNT2B were upregulated while miR-15b-5p was downregulated in serum of DN patients and HG-treated HMCs. CDKN2B-AS1 inhibition reduced HG-induced viability, cell cycle progression, ECM accumulation, and inflammation response in HMCs. CDKN2B-AS1 regulated WNT2B expression via competitively binding to miR-15b-5p. MiR-15b-5p inhibitor reversed CDKN2B-AS1 knockdown-mediated influence on viability, cell cycle progression, ECM accumulation, and inflammation response of HG-treated HMCs. The repressive effect of miR-15b-5p mimic on viability, cell cycle progression, ECM accumulation, and inflammation response of HG-treated HMCs was abolished by WNT2B overexpression. Conclusion CDKN2B-AS1 regulated HG-induced HMC viability, cell cycle progression, ECM accumulation, and inflammation response via regulating the miR-15b-5p/WNT2B axis, provided a new mechanism for understanding the development of DN.

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